Altered glycolysis triggers impaired mitochondrial metabolism and mTORC1 activation in diabetic β-cells
Chronic hyperglycemia impairs insulin secretion from pancreatic beta cells in diabetes. Here, the authors reveal that a glucose metabolite is responsible and show lowering glucose metabolism during hyperglycemia prevents loss of beta-cell function.
Main Authors: | Elizabeth Haythorne, Matthew Lloyd, John Walsby-Tickle, Andrei I. Tarasov, Jonas Sandbrink, Idoia Portillo, Raul Terron Exposito, Gregor Sachse, Malgorzata Cyranka, Maria Rohm, Patrik Rorsman, James McCullagh, Frances M. Ashcroft |
---|---|
Format: | Article |
Language: | English |
Published: |
Nature Portfolio
2022-11-01
|
Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-022-34095-x |
Similar Items
-
Metabolomics data for: Altered glycolysis triggers impaired mitochondrial metabolism and mTORC1 activation in diabetic β-cells
by: Walsby-Tickle, J, et al.
Published: (2022) -
WSSV exploits AMPK to activate mTORC2 signaling for proliferation by enhancing aerobic glycolysis
by: Peng Zhang, et al.
Published: (2023-04-01) -
Intracellular galectin-3 is a lipopolysaccharide sensor that promotes glycolysis through mTORC1 activation
by: Xing Chen, et al.
Published: (2022-12-01) -
Dopamine neuron morphology and output are differentially controlled by mTORC1 and mTORC2
by: Polina Kosillo, et al.
Published: (2022-07-01) -
mTORC1 and mTORC2 differentially promote natural killer cell development
by: Chao Yang, et al.
Published: (2018-05-01)